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[Occupational neurotoxicology due to heavy metals-especially manganese poisoning]. [Article in Japanese] - Inoue N; Emeritus professor of Kyushu University, Asagi Hospital, 2-30 1 Asagi, Onga machi, Onga-gun, Fukuoka 811-4312, Japan.

The most hazardous manganese exposures occur in mining and smelting of ore. Recently, the poisoning has been frequently reported to be associated with welding.

In occupational exposure, manganese is absorbed mainly by inhalation. Manganese preferentially accumulates in tissues rich in mitochondria. It also penetrates the blood brain barrier and accumulates in the basal ganglia, especially the globus pallidus, but also the striatum.

Manganese poisoning is clinically characterized by the central nervous system involvement including psychiatric symptoms, extrapyramidal signs, and less frequently other neurological manifestations, Psychiatric symptoms are well described in the manganese miners and include sleep disturbance, disorientation, emotional lability, compulsive acts, hallucinations, illusions, and delusions. The main characteristic manifestations usually begin shortly after the appearance of these psychiatric symptoms.

The latter neurological signs are progressive bradykinesia, dystonia, and disturbance of gait. Bradykinesia is one of the most important findings. There is a remarkable slowing of both active and passive movements of the extremities. Micrographia is frequently observed and a characteristic finding. The patients may show some symmetrical tremor, which is usually not so marked. The dystonic posture of the limbs is often accompanied by painful cramps. This attitudal hypertonia has a tendency to decrease or disappear in the supine position and to increase in orthostation. Cog-wheel rigidity is also elisited on the passive movement of all extremities. Gait disturbance is also characteristic in this poisoning. In the severe cases, cook gait has been reported. The patient uses small steps, but has a tendency to elevate the heels and to rotate them outward. He progresses without pressing on the flat of his feet, but only upon the metatarsophalangeal articulations, mainly of the fourth and fifth toes.

Increased signal in T1-weighted image in the basal ganglia has been reported in patients with the poisoning. Thus, increased signal intensities as a target site dose can be a more useful biomakers of the manganese than other biological indices such as ambient manganese concentration or blood manganese concentration on individual basis. Manganese poisoning ultimately becomes chronic. However, if the disease is diagnosed while still at the early stages and the patient is removed from exposure, the course may be reversed.

Once well established, it becomes progressive and irreversible, even when exposure is terminated. Levodopa therapy is not effective for the management of manganese poisoning.

Levodopa unresponsiveness may be useful to distinguish manganese-induced parkinsoniasm from Parkinson disease.